Mechanisms of sinoatrial node dysfunction in a canine model of pacing-induced atrial fibrillation.

ABSTRACT:

Background

The mechanism of sinoatrial node (SAN) dysfunction in atrial fibrillation (AF) is unclear.

Objective

The purpose of this study was to test the hypothesis that defective spontaneous sarcoplasmic reticulum (SR) Ca(2+) release (Ca(2+) clock) is in part responsible for SAN dysfunction in AF.

Methods

Arrhythmic events and SAN function were evaluated in pacing-induced AF dogs (n = 7) and in normal dogs (n = 19) with simultaneous intracellular calcium (Ca(i)) and membrane potential recording.

Results

AF dogs had frequent sinus pauses during Holter monitoring. Isolated right atrium (RA) from AF dogs showed slower heart rate (P = .001), longer SAN recovery time (P = .001), and longer sinoatrial conduction time (P = .003) than normal. In normal RAs, isoprotere

SUBMITTER: Joung B 

PROVIDER: S-EPMC2925681 | biostudies-literature | 2010 Jan

REPOSITORIES: biostudies-literature